In this work, we studied transgenic glial fibrillary acidic protein-IκBα-dn mice that selectively inactivate the classical nuclear factor κB pathway by overexpressing the inhibitory protein of κBα in astrocytes, under the control of glial fibrillary acidic protein promoter. We sought to determine if glial nuclear factor κB inhibition decreases formalin pain. Formalin testing was carried out on 25-35 g littermate adult male wild-type and transgenic C57Bl/6 mice. Formalin increased spinal cord c-Fos expression and glial fibrillary acidic protein immunostaining in both wild-type and transgenic mice. Transgenic glial fibrillary acidic protein-inhibitory protein of κBα-dn mice had lower duration of formalin-induced paw-licking behavior. These data support a role of glial nuclear factor κB inhibition in reducing pain after peripheral nerve inflammation.
- NF-kappa B
ASJC Scopus subject areas